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Traditional Chinese Medicine Suppresses Left Ventricular Hypertrophy by Targeting Extracellular Signal-Regulated Kinases Signali Traditional Chinese medicine suppresses left ventricular hypertrophy by targeting extracellular signal- regulated kinases signaling pathway in spontaneously hypertensive rats The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Xiong, Xingjiang, Xiaochen Yang, Lian Duan, Wei Liu, Yun Zhang, Yongmei Liu, Pengqian Wang, Shengjie Li, and Xiaoke Li. 2017. “Traditional Chinese medicine suppresses left ventricular hypertrophy by targeting extracellular signal-regulated kinases signaling pathway in spontaneously hypertensive rats.” Scientific Reports 7 (1): 42965. doi:10.1038/srep42965. http:// dx.doi.org/10.1038/srep42965. Published Version doi:10.1038/srep42965 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:32072070 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA www.nature.com/scientificreports OPEN Traditional Chinese medicine suppresses left ventricular hypertrophy by targeting Received: 10 October 2016 Accepted: 17 January 2017 extracellular signal-regulated Published: 22 February 2017 kinases signaling pathway in spontaneously hypertensive rats Xingjiang Xiong1, Xiaochen Yang1, Lian Duan1, Wei Liu2, Yun Zhang3, Yongmei Liu3, Pengqian Wang4, Shengjie Li5 & Xiaoke Li6 Chinese herbal medicine Bu-Shen-Jiang-Ya decoction (BSJYD) is reported to be beneficial for hypertension. Over expression of extracellular signal regulated kinases (ERK) pathway plays an important role in left ventricular hypertrophy (LVH). This study aimed to observe effects of BSJYD on LVH in spontaneously hypertensive rats (SHRs) and explore its possible mechanism on regulation of ERK pathway. Sixty 12-week-old SHRs were randomly allocated into 5 groups: BSJYD high dose group, middle dose group, low dose group, captopril group, and control group. Besides, a control group of Wistar-Kyoto rats was established. All rats were treated for 8 weeks. Systolic blood pressure (SBP), heart rate (HR), pathology, and left ventricular mass index (LVMI) were measured. Western blotting and Real-time PCR were used to assess the expressions of BDNF, Ras, ERK1/2, and c-fox levels. SBP and HR were significantly decreased compared with the control group and LVMI was markedly improved by BSJYD treatment in a dose-dependent manner. BSJYD inhibited the expression of BDNF, Ras, ERK1/2, and c-fox mRNA in LVH. In conclusion, BSJYD suppressed hypertension-induced cardiac hypertrophy by inhibiting the expression of ERK pathway. These changes in gene expression may be a possible mechanism by which BSJYD provides myocardial protection from hypertension. Hypertension is an important worldwide public health challenge because of its high prevalence and concomitant increase in risks of cardiovascular, cerebrovascular and renal diseases1,2. It has been identified as the leading risk factor for mortality in human populations, and is ranked third as a cause of disability-adjusted life-years3,4. Hypertension is not only manifested by an elevated arterial blood pressure (BP), but also involves complex struc- tural and functional alterations of its target organs5. In the hypertensive state, a number of adaptive changes occur in ventricle. Cardiac hypertrophy results from increased mechanical load on the heart and through the action of neurohumoral mediators. Left ventricular hypertrophy (LVH) is a cardinal manifestation of hypertensive organ damage associated with an increased cardiovascular morbidity and mortality6,7. LVH in hypertensive patients may be regarded as a powerful, independent biomarker reflecting the impact of pressure overload as well as of several risk factors on heart8. These structural abnormalities may play an important role in the development and 1Department of Cardiology, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China. 2Department of Cardiology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China. 3Department of Molecular Biology, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China. 4Department of Pharmacology, Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China. 5Department of Molecular Biology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China. 6Bio-organic and Natural Products Laboratory, McLean Hospital, Harvard Medical School, Belmont, USA. Correspondence and requests for materials should be addressed to X.X. (email: [email protected]) SCIENTIFIC REPORTS | 7:42965 | DOI: 10.1038/srep42965 1 www.nature.com/scientificreports/ Group n 0 week 4 weeks 8 weeks WKY 12 120.71 ± 8.79**▲▲ 125.98 ± 9.08**▲▲ 126.77 ± 8.54** C 12 201.73 ± 9.43 212.63 ± 8.16▲▲ 218.65 ± 9.72▲▲ Ca 12 200.66 ± 10.56 164.77 ± 8.52** 170.28 ± 10.12** Bh 12 202.27 ± 9.06 184.37 ± 10.35**▲ 178.13 ± 8.76** Bm 12 201.54 ± 10.06 193.03 ± 9.89▲ 188.04 ± 7.86**▲ Bl 12 200.81 ± 9.32 190.17 ± 8.91▲ 190.65 ± 9.79**▲ Table 1. Effect of Bu-Shen-Jiang-Ya decoction on systolic blood pressure. *P < 0.05, **P < 0.01, significantly different from the C group. ▲P < 0.05, ▲▲P <​ 0.01, significantly different from the Ca group. Group n 0 week 4 weeks 8 weeks WKY 12 366.74 ± 26.83**▲▲ 345.91 ± 25.42**▲▲ 331.77 ± 27.92** C 12 412.89 ± 19.56 396.26 ± 23.83▲▲ 370.51 ± 23.91▲▲ Ca 12 408.36 ± 20.72 391.88 ± 22.61 361.69 ± 20.07 Bh 12 402.52 ± 24.07 376.63± 23.01*▲ 344.43 ± 18.93**▲ Bm 12 399.25 ± 25.80 394.42 ± 22.80 383.74 ± 27.03▲ Bl 12 405.48 ± 21.84 391.37 ± 18.02 387.45 ± 23.91▲▲ Table 2. Effect of Bu-Shen-Jiang-Ya decoction on heart rate. *P < 0.05, **P <​ 0.01, significantly different from the C group. ▲P < 0.05, ▲▲P <​ 0.01, significantly different from the Ca group. maintenance of hypertension, because they may eventually lead to decompensation and ventricular extension, thus increasing the risk of heart failure and sudden death. Studies have confirmed that, with the development of LVH, the incidence of cardiovascular events has increased by 6–10 times9–12. Therefore, suppression of LVH was shown to improve cardiovascular outcome independently of other risk factors, and thus has been suggested as an intermediate endpoint13,14. The mitogen-activated protein kinases (MAPKs) have been implicated as focal mediators of cardiac hyper- trophy in both cell culture and genetically modified mouse models15. The extracellular signal-regulated kinase (ERK) signaling pathway, a branch of the greater MAPK signaling cascade, appears to induce a unique form of concentric cardiac hypertrophy16. It is activated in response to almost every stress- and agonist-induced hyper- trophic stimulus examined to date, suggesting the straightforward hypothesis that these kinases are required for promoting the cardiac growth response17. Signaling through ERK cascade is classically initiated at the cell membrane by activation of the small G protein Ras that then recruits the MAP3K Raf-1 to the plasma membrane, where it is activated18. More and more evidences showed that over expression of ERK signaling pathway plays an important role in cardiac hypertrophy19–21. Traditional Chinese medicine (TCM) has been reported to be effective for the treatment of hyperten- sion22–24. However, there was little information available in literature about whether Chinese herbal medicine with anti-hypertensive effect could affect ERK pathway in LVH. Herbal compounds Bu-Shen-Jiang-Ya decoction (BSJYD) has been widely used in treating hypertension with kidney yin deficiency syndrome for many years. In our previous study, a prospective case series involving 108 hypertensive patients with kidney yin deficiency syn- drome revealed a significant reduction of 13.1 mmHg of systolic blood pressure (SBP) and 9.30 mmHg of diastolic blood pressure (DBP) by BSJYD25. Additionally, no acute toxicology was identified on mice26. The significant BP-lowering effect of BSJYD has been confirmed in spontaneously hypertensive rats (SHRs); moreover, the pos- sible cardioprotective mechanisms of BSJYD on hypertension may be related to up-regulating adiponectin and improving insulin resistance27. However, further study of its detailed anti-hypertensive and reversing ventricular hypertrophy mechanism is still needed. Here, we aimed to examine how ERK signal transduction induces LVH and whether BSJYD inhibits LVH bioactivities through the ERK signaling pathway effectively. Results Effect of BSJYD on SBP. After treatment for 8 weeks, SBP was significantly decreased in the Ca group, the Bh group, the Bm group, and the Bl group compared with the C group (P <​ 0.05). Compared with the Ca group, SBP was significantly increased in the Bm group, the Bl group, and the C group (P <​ 0.05), while no significant differences were identified between the Ca group and Bh group (P >​ 0.05) (as shown in Table 1). Effect of BSJYD on HR. As shown in Table 2, HR were significantly lowered after 8 weeks in the Bh group (P <​ 0.01), while HR in the Bm group, the Bl group, and the Ca group were not significantly lowered when com- pared to the C group. As compared with the Ca group, the Bh group was significantly lowered (P < 0.05), while there is no significantly difference in the other groups (P > 0.05). Effect of BSJYD on LVMI. After treatment for 8 weeks, LVMI in the WKY group, the Ca group, and the Bh group were significantly lowered when compared to the C group (P <​ 0.05). However, no significant difference between the Ca group and Bh group was identified (Fig. 1). SCIENTIFIC REPORTS | 7:42965 | DOI: 10.1038/srep42965 2 www.nature.com/scientificreports/ Figure 1. Effect of Bu-Shen-Jiang-Ya decoction on left ventricular mass index. *P < 0.05, **P < 0.01, significantly different from the C group.
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